The effects of single-season tropospheric ozone (O3) exposures on growth, leaf abscission, and biomass of trembling aspen (Populustremuloides Michx.) rooted cuttings and seedlings were studied. Plants were grown in the Upper Peninsula of Michigan in open-top chambers with O3 exposures that ranged from 7 to 92 ppm-h. Depending on the genotype, total seasonal O3 exposure in the range of 50–92 ppm-h had negative impacts on stem, retained leaf, and root biomass accumulation and on diameter growth. Leaf abscission generally increased with increasing O3 exposure and was the principal cause of the decrease in leaf biomass of the O3-treated plants. Considerable genetic variation in O3 responses occurred, as shown by differences in sensitivities among clones and among seedlings. However, the responses to O3 of rooted cuttings and seedlings were similar when seedling means were compared with clonal means for leaf abscission, diameter growth, retained leaf biomass, and root biomass. Comparison of a single square-wave treatment (52 ppm-h) with 70 and 92 ppm-h episodic exposures suggested that the plant response to the square-wave exposure was similar to the response to the highest episodic exposure even though the 92 ppm-h episodic exposure was almost twice the square-wave exposure. Our results are consistent with previous studies that show that P. tremuloides is highly responsive to O3 exposure and this response has a strong genetic component.

Current projections indicate steady increases in both trophospheric ozone and carbon dioxide well into the next century with concurrent increases in plant stress. Because information about effects of these interacting stresses on forest trees is limited, we have conducted ozone and carbon dioxide experiments using ozone-tolerant and ozone-sensitive trembling aspen (Populustremuloides Michx.) clones (clones 216 and 259, respectively). Aspen plants were grown either in pots (square-wave study) or in the ground (episodic study) in open-top chambers. Plants in the square-wave study were exposed for a single growing season to charcoal-filtered air (CF) or to CF plus elevated carbon dioxide (CO2), ozone (O3), or O3 plus CO2 (O3 + CO2). Plants in the episodic study were exposed for three growing seasons to CF, twice simulated ambient (2x) O3 (2x O3), or 2x O3 plus CO, (2x O3 + CO2). Photosynthetic measurements were made either in the open-top chambers at treatment CO2 concentrations or in controlled-environment cuvettes with various CO2 concentrations, producing assimilation versus intercellular CO2 concentration (A/Ci) curves. Ozone decreased photosynthetic rate and stomatal conductance and accelerated leaf senescence. Elevated CO2 increased photosynthetic rate and decreased stomatal conductance when measured at treatment CO2 concentrations, and exacerbated the negative effect of O3 on photosynthesis. For example, for clone 259, photosynthesis decreased 9% for the O3 treatment compared with the CF treatment, but decreased 24% for the O3 + CO2 treatment compared with the CF treatment. Similar decreases for clone 216 of 2% and 6% for O3 and O3 + CO2, respectively, were not significant. A/Ci curves showed that O3 decreased carboxylation efficiency and maximum photosynthetic rate and that photosynthetic inhibition in response to O3 was greater with elevated CO2. The simultaneous declines in all factors of photosynthetic gas exchange measurements suggest that the equilibrium between stomatal conductance, carboxylation, and light harvesting systems was not disrupted by O3 and O3× CO2 interactions. Carbon dioxide did not ameliorate the detrimental effects of O3 on the leaf photosynthetic apparatus. In fact, the O3-tolerant clone appeared more sensitive to O3 with elevated CO2.

Background: Early, accurate diagnosis of mild traumatic brain injury (mTBI) can improve clinical outcomes for patients, but mTBI remains difficult to This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Introduction Endorphins, endocannabinoids, monoamines, and neurotrophins have all been implicated in the euphoric response to endurance running, known as a runner’s high (RH). The epitranscriptional mechanisms regulating this effect have not been defined. Here, we investigate peripheral micro–ribonucleic acid (miRNA) changes unique to athletes experiencing postrun euphoria, yielding insights into gene networks that control an RH. Methods A cohort study involving 25 collegiate runners (48% females, age = 20 ± 1 yr) examined salivary RNA levels before and after a long-distance run. Participants were divided into RH and nonrunner’s high (NRH) groups based on surveys of four criteria (mood, lost sense of time, run quality, and euphoria). Physiological measures were also recorded (temperature, heart rate, blood pressure, pupillary dilatation, and salivary serotonin). Levels of miRNAs and their messenger RNA targets were compared across pre- and postrun samples from RH and NRH groups with two-way ANOVA. Representation of opioid, gamma-aminobutyic acid (GABA), endocannabinoid, neurotrophin, serotonergic, and dopaminergic pathways was assessed in DIANA miRPath. Pearson’s correlation analyses examined relationships between miRNAs and RH indices. Results RH participants (n = 13) demonstrated postrun mydriasis (P = 0.046) and hypothermia (P = 0.043) relative to NRH participants (n = 12) but had no difference in serotonin dynamics (P = 0.88). Six miRNAs (miR-194-5p, miR-4676-3p, miR-4254, miR-4425, miR-1273-3p, miR-6743-5p) exhibited significant effects (false discovery rate P value < 0.05) across pre- or postrun and RH/NRH groups. These miRNAs displayed target enrichment for opioid (P = 2.74E−06) and GABA (P = 0.00016) pathways. miR-1237-3p levels were related with lost sense of time (R = 0.40). Mitogen-activated protein kinase (MAPK11), an endocannabinoid target of miR-1273-3p, was nominally elevated in RH participants (false discovery rate P value = 0.11). Conclusions Unique dynamics in miRNA concentration occur in athletes with subjective/objective evidence of RH, targeting genes implicated endorphin, endocannabinoid, and GABAergic signaling.